What is the main function of vitamin K in blood clotting? A Comprehensive Guide

January 8, 2026 •

3 min read

First discovered in 1929 by scientist Henrik Dam, who named it 'koagulationsvitamin,' vitamin K was quickly recognized for its vital role in the body. The main function of vitamin K in blood clotting is to act as a crucial cofactor for enzymes that activate key proteins required for the complex coagulation cascade.

Quick Summary

Vitamin K is a fat-soluble nutrient that acts as a cofactor for enzymes that modify specific coagulation factors in the liver, enabling them to bind calcium and become active.

Key Points

Cofactor for Carboxylation: Vitamin K is a crucial cofactor for the enzyme gamma-glutamyl carboxylase, which adds carboxyl groups to specific clotting proteins.
Activates Clotting Proteins: It is essential for activating specific clotting factors synthesized in the liver, including prothrombin (Factor II), Factor VII, Factor IX, and Factor X.
Enables Calcium Binding: The carboxylation reaction allows clotting factors to bind calcium ions ($Ca^{2+}$), a necessary step for their function in the blood clotting cascade.
Impairs Clotting Without It: Deficiency in vitamin K leads to the production of non-functional clotting proteins, severely impairing the body's ability to form clots and stop bleeding.
Inhibited by Warfarin: The anticoagulant drug warfarin works by blocking the enzyme that recycles vitamin K, effectively reducing the activation of clotting factors and preventing unwanted blood clots.
Recycled in the Body: The vitamin K cycle allows the body to efficiently reuse the vitamin for continuous carboxylation of clotting proteins, which is why deficiency from diet alone is rare in healthy adults.

The Core Function: Activating Clotting Factors

The primary role of vitamin K is in blood coagulation (hemostasis). It functions as a cofactor for a post-translational modification process involving vitamin K-dependent proteins, primarily clotting factors produced in the liver.

The Vitamin K Cycle and Carboxylation

Vitamin K's activation mechanism involves gamma-carboxylation.

Vitamin K is reduced to its active form by VKOR in liver cells.
GGCX uses active vitamin K to add a carboxyl group to glutamate residues on precursor clotting proteins.
This creates Gla residues.
Gla residues enable the clotting factors to bind calcium ions ($Ca^{2+}$).
Calcium binding is vital for clotting factors to function and interact with the coagulation cascade.

This cycle of reduction and re-oxidation of vitamin K ensures continuous carboxylation, meaning the body's need for the vitamin is relatively low.

The Vitamin K-Dependent Proteins

Vitamin K activates several proteins. For blood clotting, the critical ones are:

Procoagulant factors: Factor II (Prothrombin), Factor VII, Factor IX, and Factor X.
Anticoagulant proteins: Protein C and Protein S.

The Coagulation Cascade: A Multi-Step Process

The coagulation cascade is a complex series of steps leading to a fibrin clot. Vitamin K-dependent factors are essential here. For instance, Factor X helps convert prothrombin to thrombin, which forms the fibrin mesh. Insufficient active vitamin K factors impair this process, causing excessive bleeding.

Vitamin K Deficiency and Impaired Clotting

Vitamin K deficiency results in inactive clotting factors unable to bind calcium, thus hindering coagulation.

Causes of Vitamin K Deficiency

While uncommon in healthy adults, deficiency can stem from:

Fat malabsorption: Conditions like cystic fibrosis or liver disease impede absorption of fat-soluble vitamin K.
Medication: Anticoagulants like warfarin block the vitamin K cycle by inhibiting VKOR.
Diet: Extremely poor diets low in leafy greens can contribute, though rare.
Neonatal risk: Newborns are susceptible to VKDB due to lack of gut bacteria producing K2 and poor placental transfer. They often receive a prophylactic injection.

Symptoms and Consequences

Deficiency symptoms vary and can include:

Easy bruising and gum bleeding.
Excessive bleeding from injuries.
Gastrointestinal bleeding.
Intracranial hemorrhage in infants.

Comparison: Vitamin K1 vs. Vitamin K2


Feature	Vitamin K1 (Phylloquinone)	Vitamin K2 (Menaquinones)
Source	Found in green leafy vegetables.	Synthesized by gut bacteria and in fermented foods.
Absorption	Absorbed in the small intestine.	Absorbed from gut bacteria and foods.
Function	Primarily activates liver clotting factors.	Also involved in liver clotting but has roles in bone and arteries.

How Blood-Thinning Medications Interact with Vitamin K

Anticoagulants, like warfarin, inhibit clotting. Warfarin specifically blocks VKOR, disrupting the vitamin K cycle and preventing activation of clotting factors. This reduces clotting ability, lowering clot risk. Patients on warfarin must manage their vitamin K intake to maintain drug effectiveness.

Conclusion

Vitamin K is essential for blood clotting, acting as a cofactor for the carboxylation of specific liver proteins. This enables factors like prothrombin and Factor VII to bind calcium and function in the coagulation cascade. Without this, the body's ability to stop bleeding is severely hindered. Adequate intake and understanding its function are vital for healthy hemostasis. For more information on dietary recommendations, consult the NIH Fact Sheet on Vitamin K.

Frequently Asked Questions

Vitamin K acts as a cofactor for the enzyme gamma-glutamyl carboxylase, which modifies specific clotting factors in the liver. This modification allows these factors to bind calcium, a necessary step for their activation and function in the blood clotting cascade.

The most important vitamin K-dependent clotting factors are Factor II (Prothrombin), Factor VII, Factor IX, and Factor X. The anticoagulant proteins C and S also depend on vitamin K for their function.

A vitamin K deficiency impairs the activation of clotting factors, leading to a reduced ability to form blood clots. This can result in easy bruising, excessive bleeding from wounds, and, in severe cases, dangerous hemorrhage.

Warfarin, a common anticoagulant, works by inhibiting the enzyme vitamin K epoxide reductase (VKOR), which is responsible for recycling vitamin K. By blocking this recycling, warfarin prevents the activation of vitamin K-dependent clotting factors, thereby reducing blood clotting.

In healthy adults with a balanced diet, vitamin K deficiency is rare because it is found in many foods and is also produced by bacteria in the gut. However, individuals with fat malabsorption disorders, liver disease, or those taking certain medications are at higher risk.

Both Vitamin K1 and K2 are crucial for the liver's production of clotting factors. Vitamin K1, from plants, is directed towards the liver for this process, while Vitamin K2, from bacteria and fermented foods, also contributes but may have additional roles in other tissues like bone and arteries.

Vitamin K1 is abundant in green leafy vegetables such as kale, spinach, and broccoli. Vitamin K2 can be found in fermented foods like natto and some cheeses, as well as being produced by gut bacteria.